Neuropathology — MCQs

Neuropathology Indian Medical PG Practice Questions and MCQs

Question 81: A 10-year-old boy presents with increasing muscle weakness and elevated creatine phosphokinase (CPK) levels. What is the most likely structure with a defect causing these symptoms?

A. Nerves
B. Muscle fibers (Correct Answer)
C. Basement membrane
D. All body cells

Explanation: **Explanation:** The clinical presentation of a 10-year-old boy with progressive muscle weakness and elevated Creatine Phosphokinase (CPK) is classic for **Duchenne Muscular Dystrophy (DMD)** [1]. DMD is caused by a mutation in the *DMD* gene, which encodes **dystrophin**, a critical structural protein located on the cytoplasmic side of the **sarcolemma (muscle fiber membrane)**. **1. Why Muscle Fibers are the correct answer:** Dystrophin acts as a mechanical link between the intracellular actin cytoskeleton and the extracellular matrix. A defect in this protein leads to membrane instability, causing muscle fiber necrosis during contraction [1]. This damage results in the leakage of intracellular enzymes, such as **CPK**, into the bloodstream [2]. Therefore, the primary defect resides within the structural integrity of the muscle fibers. **2. Why other options are incorrect:** * **Nerves:** Defects in nerves (e.g., Spinal Muscular Atrophy) cause neurogenic atrophy. While weakness occurs, CPK levels are typically normal or only mildly elevated, unlike the massive elevations seen in primary myopathies [2]. * **Basement membrane:** While dystrophin links to the basement membrane via the dystroglycan complex, the primary molecular defect in DMD/BMD is the absence or abnormality of the dystrophin protein within the muscle fiber itself. * **All body cells:** The *DMD* gene expression is primarily localized to skeletal muscle, cardiac muscle, and some specialized neurons. It is not a generalized defect affecting every cell in the body. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** X-linked recessive (most common and severe muscular dystrophy). * **Gower’s Sign:** Use of hands to "climb up" the legs to stand, indicating proximal muscle weakness. * **Pseudohypertrophy:** Calf enlargement due to replacement of muscle with fibrofatty tissue. * **Diagnosis:** Gold standard is Genetic Testing; Muscle biopsy shows variation in fiber size and increased endomysial fibrosis [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1244-1245. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1239-1240.

Question 82: What is the most common intracranial neoplasm in adults?

A. Meningioma
B. Astrocytoma (Correct Answer)
C. Posterior fossa tumor
D. Ganglioneuroma

Explanation: **Explanation:** The most common primary intracranial neoplasm in adults is the **Astrocytoma** [1]. This group of tumors arises from astrocytes (glial cells) and represents the majority of primary brain parenchymal tumors [1]. Within this category, **Glioblastoma Multiforme (GBM)**—a Grade IV astrocytoma—is the most frequent and aggressive subtype seen in the adult population [2]. **Analysis of Options:** * **Astrocytoma (Correct):** Glial tumors (Gliomas) account for approximately 80% of all primary malignant brain tumors. Among these, astrocytomas are the most prevalent [1]. * **Meningioma:** While Meningiomas are the most common *extra-axial* (benign) intracranial tumors, they are generally ranked second to gliomas when considering overall primary intracranial neoplasms in many clinical classifications. * **Posterior Fossa Tumor:** These are more characteristic of the **pediatric** population (e.g., Medulloblastoma, Pilocytic Astrocytoma) [1]. In adults, the majority of tumors are supratentorial. * **Ganglioneuroma:** These are rare, slow-growing tumors composed of mature neuronal elements and are not among the common intracranial neoplasms. **NEET-PG High-Yield Pearls:** 1. **Overall Most Common:** If the question asks for the most common brain tumor overall (including secondary), the answer is **Metastasis** (usually from lung, breast, or melanoma). 2. **Location Rule:** Adult brain tumors are typically **Supratentorial**, whereas pediatric brain tumors are typically **Infratentorial** (Posterior Fossa). 3. **GBM Hallmark:** Look for "pseudopalisading necrosis" and "vascular endothelial proliferation" on histopathology [2]. 4. **Meningioma Hallmark:** Look for "Psammoma bodies" and "Whorled pattern" on histology; these are often associated with NF-2. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 725-726. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1308-1310.

Question 83: Which of the following tumors has the best prognosis?

A. Cerebellar pilocytic astrocytoma (Correct Answer)
B. Grade IV astrocytoma
C. Medulloblastoma
D. Ependymoma

Explanation: **Explanation:** The correct answer is **Cerebellar Pilocytic Astrocytoma (Option A)**. **1. Why it is correct:** Pilocytic Astrocytoma is classified as a **WHO Grade I** tumor. It is the most common brain tumor in children and is characterized by its slow growth and circumscribed nature [3]. Because it is often cystic with a mural nodule and lacks the infiltrative properties of higher-grade gliomas, it is frequently curable by surgical resection alone. The 10-year survival rate exceeds 90%, giving it the best prognosis among the listed options. **2. Why the other options are incorrect:** * **Grade IV Astrocytoma (Glioblastoma):** This is the most malignant primary brain tumor [1]. It is highly aggressive, infiltrative, and associated with a very poor prognosis (median survival is often <15 months) [1]. * **Medulloblastoma:** This is a **WHO Grade IV** embryonal tumor. While it is radiosensitive and survival rates have improved with multimodal therapy, it remains a highly malignant tumor with a significant risk of CSF seeding ("drop metastasis") [2]. * **Ependymoma:** These are typically **WHO Grade II or III** tumors [4]. While less aggressive than Glioblastoma, their location (often the floor of the 4th ventricle) makes complete surgical resection difficult, leading to a higher risk of recurrence compared to pilocytic astrocytomas [4]. **3. NEET-PG High-Yield Pearls:** * **Morphology:** Look for **Rosenthal fibers** (thick, eosinophilic, corkscrew-shaped structures) and bipolar cells with long hair-like processes ("pilocytic"). * **Imaging:** Classically presents as a **cystic lesion with a contrast-enhancing mural nodule** in the posterior fossa. * **Genetics:** Frequently associated with **BRAF gene** alterations (KIAA1549-BRAF fusion). * **Marker:** Strongly GFAP (Glial Fibrillary Acidic Protein) positive [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1310-1311. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1314-1315. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 725-726. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1312-1313.

Question 84: Which area of the brain is involved in Alzheimer's disease?

A. Cerebral cortex
B. Hippocampus
C. Cerebellum
D. Cerebral cortex and Hippocampus (Correct Answer)

Explanation: **Explanation:** Alzheimer’s Disease (AD) is the most common cause of dementia in the elderly, characterized by the progressive accumulation of Amyloid-beta (Aβ) plaques and Tau-containing neurofibrillary tangles [2]. **Why Option D is Correct:** The pathology of Alzheimer’s follows a specific anatomical progression. The **Hippocampus** (and the entorhinal cortex) is typically the first area to undergo significant atrophy, explaining why **short-term memory loss** is the earliest clinical symptom [2]. As the disease progresses, the pathology spreads to the **Cerebral Cortex** (specifically the frontal, temporal, and parietal lobes), leading to cognitive decline, language deficits (aphasia), and loss of executive function [2]. Therefore, both areas are fundamentally involved. **Analysis of Incorrect Options:** * **A & B:** While both are involved, selecting one over the other is incomplete. The disease is defined by the involvement of the limbic system (hippocampus) for memory and the neocortex for higher cognitive functions. * **C. Cerebellum:** The cerebellum is characteristically **spared** in Alzheimer’s disease [2]. Motor functions and coordination usually remain intact until the very terminal stages of the illness. **NEET-PG High-Yield Pearls:** * **Gross Pathology:** Symmetrical cortical atrophy, compensatory ventricular enlargement (**Hydrocephalus ex-vacuo**), and "knife-edge" thinning of gyri with widening of sulci [1]. * **Microscopic Hallmarks:** 1. **Neuritic (Senile) Plaques:** Extracellular Aβ42 deposits (stained with Congo Red/Silver stain) [3]. 2. **Neurofibrillary Tangles (NFTs):** Intracellular hyperphosphorylated **Tau protein** [1]. * **Hirano Bodies:** Eosinophilic, actin-rich inclusions found in hippocampal pyramidal cells. * **Genetics:** Early-onset is associated with **APP** (Chr 21), **Presenilin 1** (Chr 14), and **Presenilin 2** (Chr 1); Late-onset is associated with **ApoE4** (Chr 19) [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1294-1295. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 720-721. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1290-1292.

Question 85: Brain edema is associated with which of the following?

A. Increase in extracellular fluid volume (Correct Answer)
B. Increase in brain water content
C. Increase in volume in the interstitial space
D. None of the above

Explanation: **Explanation:** Brain edema is defined as an abnormal accumulation of fluid within the brain parenchyma, leading to a volumetric increase in brain tissue. **1. Why Option A is Correct:** The core mechanism of brain edema involves the expansion of the **extracellular fluid (ECF) volume**. In the most common type, **Vasogenic Edema**, there is a disruption of the Blood-Brain Barrier (BBB). This allows intravascular fluid and plasma proteins to leak into the extracellular spaces between neurons and glial cells. While "brain water content" increases globally, the specific pathological hallmark that characterizes the expansion of the tissue is the increase in the extracellular compartment. **2. Why Other Options are Incorrect:** * **Option B (Increase in brain water content):** While technically true that water content increases, this is a general physiological observation rather than the specific pathological definition used in medical literature to describe the fluid shift. In pathology, we focus on the *compartmental* shift (ECF vs. ICF). * **Option C (Increase in volume in the interstitial space):** This is a subset of extracellular fluid. However, in **Cytotoxic Edema**, the fluid accumulates *intracellularly* (within neurons and glia) due to Na+/K+ pump failure. Since "Extracellular Fluid Volume" (Option A) is a broader term that encompasses the primary mechanism of the most common form (Vasogenic), it is the preferred academic answer. **High-Yield Clinical Pearls for NEET-PG:** * **Vasogenic Edema:** Most common; occurs in tumors/abscesses; fluid is in the **extracellular space**; affects **white matter** more than grey matter. * **Cytotoxic Edema:** Occurs in ischemia/hypoxia; fluid is **intracellular** (cell swelling); affects both white and grey matter. * **Interstitial (Hydrocephalic) Edema:** Seen in obstructive hydrocephalus; fluid moves from ventricles into periventricular white matter [1]. * **Morphology:** On gross examination, gyri are flattened, sulci are narrowed, and the brain feels soft [2]. (Note: While the provided references primarily discuss Hydrocephalus and herniation, Reference explicitly titles the section encompassing cerebral edema and raised pressure, and Reference illustrates the gross effect of a swollen brain leading to herniation.) **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1256-1257. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 699-700.

Question 86: Lisch nodule is seen in which of the following conditions?

A. Neurofibromatosis (Correct Answer)
B. Tuberous sclerosis
C. Von-Hippel-Lindau syndrome
D. Tumor metastasis to brain

Explanation: **Explanation:** **Lisch nodules** are pigmented hamartomatous nodular aggregates of dendritic melanocytes located in the iris. They are a hallmark clinical feature of **Neurofibromatosis Type 1 (NF1)**, also known as von Recklinghausen disease. These nodules appear as well-defined, dome-shaped, light brown to yellow elevations on the iris surface. While they do not affect vision, they are highly sensitive and specific diagnostic markers, present in over 95% of affected individuals after age 10. **Analysis of Options:** * **Neurofibromatosis (Correct):** Specifically associated with NF1 (Chromosome 17) [2]. Other key features include Café-au-lait spots, neurofibromas, optic gliomas, and axillary freckling (Crowe sign) [2]. * **Tuberous Sclerosis:** Characterized by the triad of seizures, mental retardation, and adenoma sebaceum [3]. Ocular findings typically include **retinal astrocytic hamartomas** (mulberry lesions) [3], not Lisch nodules. * **Von-Hippel-Lindau (VHL) Syndrome:** Associated with hemangioblastomas of the retina and cerebellum. The classic ocular finding is **retinal capillary hemangioblastoma**. * **Tumor Metastasis:** Metastases to the eye most commonly affect the choroid (due to high vascularity) rather than the iris, and they present as destructive masses rather than discrete hamartomatous nodules. **High-Yield Clinical Pearls for NEET-PG:** * **NF1 vs. NF2:** Lisch nodules are characteristic of **NF1**. They are generally **absent in NF2** [1]. * **NF2 Ocular Finding:** The classic ocular sign for NF2 is **Juvenile posterior subcapsular lenticular opacity** (cataract). * **Genetics:** NF1 involves the *NF1* gene on **Chromosome 17** (encodes Neurofibromin); NF2 involves the *merlin* gene on **Chromosome 22** [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 727-728. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1249-1250. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1318-1319.

Question 87: Which of the following carcinomas most frequently metastasizes to the brain?

A. Small cell carcinoma of the lung (Correct Answer)
B. Prostate cancer
C. Rectal carcinoma
D. Endometrial cancer

Explanation: **Explanation:** Brain metastases are the most common intracranial tumors in adults, occurring much more frequently than primary brain malignancies. Among all cancers, **Lung Carcinoma** is the most common primary source of brain metastasis [1] (accounting for approximately 40-50% of cases). **Why Small Cell Carcinoma of the Lung is correct:** Small cell carcinoma of the lung (SCLC) has an exceptionally high propensity for early hematogenous spread [2]. By the time of diagnosis, micro-metastases to the brain are so common that prophylactic cranial irradiation (PCI) is often part of the standard treatment protocol [3]. While adenocarcinoma is the most common *subtype* of lung cancer to metastasize to the brain in absolute numbers (due to its higher overall incidence), SCLC has the highest *relative frequency* and aggressiveness regarding CNS involvement. **Analysis of Incorrect Options:** * **B. Prostate Cancer:** Rarely metastasizes to the brain parenchyma [1]; it more commonly spreads to the pelvic lymph nodes and bone (osteoblastic metastases). * **C. Rectal Carcinoma:** While GI cancers can spread to the brain [1], they typically metastasize to the liver (via portal circulation) or lungs first. * **D. Endometrial Cancer:** CNS involvement is extremely rare and usually occurs only in the setting of widely disseminated FIGO Stage IV disease. **High-Yield Clinical Pearls for NEET-PG:** * **Order of frequency for Brain Metastasis:** Lung > Breast > Melanoma > Renal Cell Carcinoma > Colon [1]. * **Melanoma** has the highest *likelihood* of spreading to the brain per case [1], but Lung cancer is the most common *overall* due to its high prevalence. * **Location:** Metastases typically occur at the **grey-white matter junction** (where caliber of blood vessels narrows, trapping tumor emboli). * **Radiology:** Often present as multiple, well-circumscribed lesions with significant perilesional edema. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1317-1318. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 337-338. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 338-339.

Question 88: Meningioma arises from which of the following cell types?

A. Extra dural arteries
B. Extra cranial muscles
C. Venous sinuses
D. Arachnoid cap cells (Correct Answer)

Explanation: **Meningiomas** are the most common primary intracranial tumors in adults. They are typically slow-growing, benign (WHO Grade 1) tumors that arise from the **arachnoid cap cells** (also known as meningothelial cells) [1]. These cells are found in the arachnoid granulations, which are specialized structures that project into the dural venous sinuses to facilitate CSF resorption. * **Why Option D is Correct:** Arachnoid cap cells are the cells of origin for meningiomas [1]. These cells are most concentrated near the venous sinuses, which explains why meningiomas are frequently found in the parasagittal region and the convexity of the brain. * **Why Options A, B, and C are Incorrect:** * **Extra dural arteries** (like the middle meningeal artery) are associated with epidural hematomas, not primary tumors. * **Extra cranial muscles** do not contribute to intracranial meningeal pathology. * **Venous sinuses** are the *location* where arachnoid granulations are found, but the sinuses themselves (endothelial lining) do not give rise to meningiomas. **High-Yield Facts for NEET-PG:** * **Epidemiology:** More common in females (2:1 ratio) due to the presence of **progesterone receptors** on the tumor cells. * **Genetics:** Frequently associated with **NF2 (Neurofibromatosis type 2)**; the most common genetic mutation involves the *merlin* gene on chromosome 22 [1][2]. * **Histopathology:** Characterized by **whorled patterns** of cells and the presence of **Psammoma bodies** (laminated calcifications) [2][3]. * **Imaging:** Classically shows a **"Dural Tail Sign"** on contrast-enhanced MRI, representing reactive dural thickening [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1319-1320. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 727-728. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1316-1317.

Question 89: Disease or infarction of neurological tissue causes it to be replaced by what?

A. Fluid
B. Neuroglia (Correct Answer)
C. Proliferation of adjacent nerve cells
D. Blood vessel

Explanation: **Explanation:** In the Central Nervous System (CNS), the response to injury or infarction differs significantly from peripheral tissues. While most organs undergo **fibrosis** (scarring by fibroblasts and collagen), the brain lacks significant connective tissue. Instead, it undergoes **Gliosis** [3]. **Why Neuroglia is correct:** When neural tissue is damaged, specialized glial cells called **Astrocytes** undergo hypertrophy and hyperplasia [3]. This process, known as **astrogliosis**, results in the formation of a "glial scar." These astrocytes proliferate to wall off the damaged area, effectively replacing the lost neurons [3]. This is the CNS equivalent of scarring. **Analysis of Incorrect Options:** * **A. Fluid:** While chronic infarcts eventually result in **liquefactive necrosis** (forming a cystic cavity filled with fluid) [1], the structural replacement and "healing" mechanism itself is the proliferation of neuroglia. * **C. Proliferation of adjacent nerve cells:** This is incorrect because neurons are **permanent cells**. They are post-mitotic and do not have the regenerative capacity to proliferate or replace lost tissue [3]. * **D. Blood vessel:** While angiogenesis (neovascularization) occurs during the early stages of repair (granulation-like tissue), it does not replace the bulk of the lost neurological tissue. **High-Yield NEET-PG Pearls:** 1. **Type of Necrosis:** Brain infarction uniquely leads to **Liquefactive Necrosis** (unlike the coagulative necrosis seen in the heart or kidneys) [1]. 2. **Key Marker:** The hallmark of gliosis is the increased expression of **GFAP (Glial Fibrillary Acidic Protein)** within astrocytes. 3. **Microglia:** These are the resident macrophages of the CNS (derived from mesoderm) that clear debris (Gitter cells) before gliosis sets in [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1268-1269. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1255-1256. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 697-698.

Question 90: Knife-edge pattern of neuronal atrophy is associated with which of the following degenerative diseases?

A. Alzheimer's disease
B. Frontotemporal dementia
C. Pick's disease (Correct Answer)
D. Progressive supranuclear palsy

Explanation: **Explanation:** **Pick’s Disease** (a subtype of Frontotemporal Lobar Degeneration) is characterized by severe, circumscribed atrophy of the frontal and temporal lobes. This profound loss of parenchyma leads to the thinning of the gyri to the extent that they resemble the sharp blade of a knife, a classic morphological finding known as **"Knife-edge atrophy."** [1] Microscopically, it is identified by **Pick bodies** (round, silver-staining cytoplasmic inclusions of 3R tau protein) and **Pick cells** (swollen, achromatic neurons). [1] **Analysis of Incorrect Options:** * **Alzheimer’s Disease:** While it involves generalized cortical atrophy, it typically presents with widening of the sulci and compensatory ventricular enlargement (hydrocephalus ex vacuo), but the gyri do not reach the extreme "knife-edge" sharpness seen in Pick’s. [2] * **Frontotemporal Dementia (FTD):** This is an umbrella term. While Pick’s disease is a form of FTD, "Pick’s disease" is the specific pathological diagnosis associated with the classic "knife-edge" description in medical literature and exams. [1] * **Progressive Supranuclear Palsy (PSP):** This is a tauopathy primarily affecting the brainstem (midbrain), subthalamic nucleus, and dentate nucleus, rather than causing the specific pattern of cortical knife-edge atrophy. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Triad of Pick’s:** Early personality changes, behavioral disinhibition, and language impairment (aphasia), often preceding memory loss. * **Sparing:** Classically spares the posterior two-thirds of the superior temporal gyrus. [1] * **Tau Protein:** Pick bodies contain **3R Tau** (Three-repeat tau), whereas Alzheimer’s contains both 3R and 4R Tau. * **Imaging:** Look for the "Asymmetric" or "Fronto-temporal" focal atrophy on MRI. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1294-1295. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 720-721.

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Cellular Pathology of the Nervous System

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Cerebrovascular Diseases

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Trauma to the Central Nervous System

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Infections of the Nervous System

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Demyelinating Diseases

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Neurodegenerative Diseases

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CNS Tumors

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Peripheral Nerve Disorders

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Neuromuscular Junction Diseases

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Congenital and Developmental Disorders

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